fos protooncogene and the regulation of gene expression in adipocyte differentiation.

Spiegelman, Bruce M.; Distel, R; Ro, Hyo‐Sung; Rosen, Barry; Satterberg, Brett

doi:10.1083/jcb.107.3.829

Cited by 32 publications

(5 citation statements)

References 28 publications

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“…Growth factors induce the expression of the nuclear proto-oncogen c-fos (Greenberg and Ziff, 1984;Kruijer et al, 19841, which has been shown to play a crucial role in adipocyte differentiation (Distel et al, 1987;Spiegelman et al, 1988). Furthermore, it is assumed that the rapid and transient increase in c-fos mRNA levels in response to mitogenic stimuli initiates the mitogenic response (Muller, 1986).…”

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confidence: 99%

The signaling potential of the receptors for insulin and insulin‐like growth factor I (IGF‐I) in 3t3‐l1 adipocytes: Comparison of glucose transport activity, induction of oncogene c‐fos, glucose transporter mRNA, and DNA‐synthesis

Weiland

Bahr

Höhne

et al. 1991

Journal Cellular Physiology

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The receptors for insulin and insulin-like growth factor I (IGF-I) have in common a high sequence homology and diverse overlapping functions, (e.g., the stimulation of acute metabolic events and the induction of cell growth.). In the present study, we have compared the potential of insulin and IGF-I receptors in stimulating glucose transport activity, glucose transporter gene expression, DNA-synthesis, and expression of proto-oncogene c-fos in 3T3-L1 adipocytes which express high levels of both receptors. Binding of both hormones to their own receptors was highly specific as compared with binding to the respective other receptor (insulin receptor: KD = 3.6 nM, KI of IGF-I greater than 500 nM; IGF-I receptor, KD = 1.1 nM, KI of insulin = 191 nM). Induction of proto-oncogene c-fos mRNA by insulin and IGF-I paralleled their respective receptor occupancy and was thus induced by both hormones via their own receptor (EC50 of insulin, 3.7; IGF-I, 3.9 nM). Similarly, both insulin and IGF-I increased DNA synthesis (EC50 of insulin, 5.8 nM; IGF-I, 4.0 nM), glucose transport activity (EC50 of insulin, 1.7 nM; IGF-I, 1.4 nM), and glucose transporter (GLUT4) mRNA levels in concentrations corresponding with their respective receptor occupancy. These data indicate that in 3T3-L1 cells the alpha-subunits of insulin and IGF-I receptors have an equal potential to stimulate a metabolic and a mitogenic response.

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mentioning

confidence: 99%

The signaling potential of the receptors for insulin and insulin‐like growth factor I (IGF‐I) in 3t3‐l1 adipocytes: Comparison of glucose transport activity, induction of oncogene c‐fos, glucose transporter mRNA, and DNA‐synthesis

Weiland

Bahr

Höhne

et al. 1991

Journal Cellular Physiology

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“…The establishment of several adipogenic cell lines able to undergo differentiation in vitro into fully mature adipocytes has provided model systems to investigate the process of differentiation at the cellular and molecular levels (1)(2)(3). Using these cell lines, several hormones and growth factors have been shown to have adipogenic (3)(4)(5) or antiadipogenic activities (6)(7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

Physiological role of epidermal growth factor on adipose tissue development in vivo.

Serrero

Mills

1991

Proc. Natl. Acad. Sci. U.S.A.

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The ability of epidermal growth factor (EGF) to affect adipose tissue development in vivo was investigated. The subcutaneous administration of EGF to newborn NBR rats for 10 days resulted in decreased body weight and fat pad weight that occurred in a dose-dependent fashion. At a dose of 1 ,Ig/g of body weight, injected EGF resulted in a 50% decrease of fat pad weight. Although kidney weight was also diminished, the weight of other organs such as liver and intestine remained unchanged or even slightly increased, suggesting that the effect of EGF on fat pad development was not due to a generalized inhibitory action of EGF on the development of the neonate rats. The number of adipocyte precursors in inguinal fat pads of EGF-treated animals was higher than in control animals (1.3-fold for 0.3 jtg/g of body weight of EGF and 1.8-fold for 1.0 jtg/g of body weight), whereas the number of mature adipocytes and the amount of triglyceride accumulated per fat pad were concomitantly lower. Adipocyte precursors isolated from EGF-treated animals displayed a reduced differentiation ability in culture and a higher sensitivity to the inhibitory effect of EGF than did cells isolated from control animals. These experiments demonstrate that EGF can retard adipose tissue development in vivo and suggest that EGF plays an important physiological role in the control of adipocyte differentiation.

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“…The AP‐1 transcription factor consists of a heterodimer of proteins belonging to the c‐Fos, c‐Jun, Jun dimerizing protein (JDP), and activating transcription factor (ATF) families. The contribution of c‐Fos to the expression of specific adipogenic genes has long been recognized (Distel et al, 1987; Distel and Spiegelman, 1988; Spiegelman et al, 1988), however, it has not been linked to regulation of PPARγ2 gene expression during adipogenic differentiation. ChIP experiments determined that c‐Fos bound to the promoter as early as 1 h post‐differentiation (Fig.…”

Section: Resultsmentioning

confidence: 99%

Chromatin accessibility and transcription factor binding at the PPARγ2 promoter during adipogenesis is protein kinase A‐dependent

Xiao

LeBlanc

et al. 2010

Journal Cellular Physiology

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The nuclear hormone receptor peroxisome proliferator activated receptor gamma (PPARγ) is a ligand-activated transcription factor that specifies formation of the adipocyte lineage. PPARγ also serves as a primary target for the treatment of type 2 diabetes, illustrating both its medical relevance as well as the need to understand fundamental aspects of PPARγ expression and function. Here, we characterize molecular changes that occur at the PPARγ2 promoter within the first several hours of adipocyte differentiation in culture. Our results demonstrate that changes in chromatin accessibility at the PPARγ2 promoter and occupancy of the promoter by the c-Fos transcription factor occur within an hour of the onset of differentiation, followed closely by the binding of the CCAAT/Enhancer Binding Protein beta (C/EBPβ) transcription factor. All three events show a remarkable dependency on protein kinase A (PKA) activity. These results reflect novel requirements for the PKA signaling pathway and reinforce the importance of PKA function during the onset of adipocyte differentiation.

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fos protooncogene and the regulation of gene expression in adipocyte differentiation.

Cited by 32 publications

References 28 publications

The signaling potential of the receptors for insulin and insulin‐like growth factor I (IGF‐I) in 3t3‐l1 adipocytes: Comparison of glucose transport activity, induction of oncogene c‐fos, glucose transporter mRNA, and DNA‐synthesis

The signaling potential of the receptors for insulin and insulin‐like growth factor I (IGF‐I) in 3t3‐l1 adipocytes: Comparison of glucose transport activity, induction of oncogene c‐fos, glucose transporter mRNA, and DNA‐synthesis

Physiological role of epidermal growth factor on adipose tissue development in vivo.

Chromatin accessibility and transcription factor binding at the PPARγ2 promoter during adipogenesis is protein kinase A‐dependent

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